Brain, behavior, & immunity - health最新文献

{"title":"Neuroinflammation and insulin resistance in major depression and bipolar disorder: Implications for clinical trials evaluating immunometabolic targeted therapies","authors":"Folkert H. van Bruggen ,&nbsp;Roger S. McIntyre","doi":"10.1016/j.bbih.2025.101166","DOIUrl":"10.1016/j.bbih.2025.101166","url":null,"abstract":"<div><div>Bipolar disorder (BD) and major depressive disorder (MDD) are highly prevalent, disabling psychiatric illnesses marked by substantial heterogeneity and frequent metabolic and inflammatory comorbidities. Growing evidence implicates low-grade inflammation, immune dysregulation, and insulin resistance (IR) in the pathophysiology, progression, and treatment response of mood disorders. While numerous clinical trials have investigated immunometabolic targeted interventions, outcomes have been inconsistent, due to limited stratification of participants based on underlying biology. This perspective paper aims to identify practical biomarkers and biosignatures to guide patient selection and optimize immunometabolic trial design. We summarize evidence linking neuroinflammation and IR to illness burden, discuss clinical trials targeting these mechanisms, and highlight emerging markers, including extracellular vesicles, monocyte gene expression profiles, and neuron-derived vesicle signatures of IR. No single validated biomarker for identification of immunometabolic phenotype currently exists, but multimodal biosignatures combining genetic, epigenetic, proteomic, and clinical features offer a pragmatic empirical path forward. Integrating these markers with advanced analytic approaches, such as machine learning, holds promise for identifying biologically coherent subgroups most likely to benefit from targeted immunometabolic interventions, accelerating precision medicine for BD and MDD.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"51 ","pages":"Article 101166"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145939123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Perceived stress precedes declines in Well-being: A prospective study of stress, well-being, hair cortisol, and low-grade inflammation in hospital employees","authors":"Monica T. Jones ,&nbsp;Rachael A. Cronin ,&nbsp;Mathew D. Marques ,&nbsp;Matthias Weigl ,&nbsp;Nicolas Rohleder ,&nbsp;Linda Becker ,&nbsp;Helena C. Kaltenegger ,&nbsp;Bradley J. Wright","doi":"10.1016/j.bbih.2025.101158","DOIUrl":"10.1016/j.bbih.2025.101158","url":null,"abstract":"<div><h3>Objective</h3><div>Chronic low-grade inflammation may help explain the relationship between stress, well-being, and disease, but the pathway and temporal order have not yet been tested prospectively. To understand the pathways between perceived stress, well-being, C-reactive protein, and hair cortisol, we investigated the temporal ordering of these variables in a sample of hospital employees.</div></div><div><h3>Methods</h3><div>Random-intercepts cross-lagged panel models were conducted using three 6-monthly waves of data collected from new employees at a German hospital (<em>N</em> = 296, 77.7 % female, M age = 28.59) in a prospective cohort study. Self-reported data on perceived stress and well-being, hair strands for hair cortisol concentration, and capillary blood samples for C-reactive protein were collected for analysis.</div></div><div><h3>Results</h3><div>While our study did not support a causal relationship between changes in stress levels and later changes in either hair cortisol or low-grade inflammation, we provide evidence to suggest that increases in perceived stress led to later decreases in well-being. In contrast, changes in well-being did not predict changes in perceived stress levels.</div></div><div><h3>Conclusion</h3><div>This is the first prospective repeated-measure study to examine the temporal associations between stress, well-being, hair cortisol concentrations, and chronic low-grade inflammation. Our analyses suggest that perceived stress in this sample precedes changes in well-being, highlighting the importance of prevention and early intervention.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"51 ","pages":"Article 101158"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145798680","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Body talk: Correlates of gut-immune dysregulation phenotypes in people living with HIV who use methamphetamine","authors":"Wilson Vincent ,&nbsp;Annesa Flentje ,&nbsp;Benjamin S. Dominguez ,&nbsp;Robert H. Paul ,&nbsp;Savita Pahwa ,&nbsp;Suresh Pallikkuth ,&nbsp;Margaret Roach ,&nbsp;Dietmar Fuchs ,&nbsp;Samantha E. Dilworth ,&nbsp;Torsten B. Neilands ,&nbsp;Peter W. Hunt ,&nbsp;Gowri Sunder ,&nbsp;Cody Lentz ,&nbsp;Sydney Telaak ,&nbsp;Adam W. Carrico","doi":"10.1016/j.bbih.2025.101156","DOIUrl":"10.1016/j.bbih.2025.101156","url":null,"abstract":"<div><h3>Background</h3><div>Microbial translocation, immune activation, inflammation, and dysregulated metabolism of neurotransmitter precursors are interacting pathophysiologic processes linked to neuropsychiatric comorbidities and faster HIV disease progression. We examined correlates of distinct phenotypes of gut-immune dysregulation in people living with HIV (PWH) who use methamphetamine.</div></div><div><h3>Methods</h3><div>Participants were 122 PWH who had biochemically confirmed recent methamphetamine use, including non-injection use. Peripheral plasma markers reflected: intestinal permeability, microbial translocation, immune activation, inflammation, and dysregulated metabolism of neurotransmitter precursors. Using latent profile analysis (i.e., clustering) of these markers, we identified gut-immune phenotypes and their clinical, demographic, and stigma-related correlates.</div></div><div><h3>Results</h3><div>Three immune profiles emerged: (1) <em>low gut-immune dysregulation</em> with lower microbial translocation, macrophage activation, inflammation, and tryptophan catabolism; (2) <em>moderate gut-immune dysregulation</em> with all markers within average range; and (3) <em>high gut-immune dysregulation</em> with higher microbial translocation, immune activation, inflammation, and tryptophan catabolism. In adjusted analyses, higher viral load (one log10 copy/ml; <em>AOR</em> = 1.97, 95 % CI = 1.02–3.82), injection of methamphetamine (<em>AOR</em> = 3.60, 95 % CI = 1.23–10.50), and internalized stigma (<em>AOR</em> = 1.78, 95 % CI = 1.01–3.15) were associated with having a moderate gut-immune dysregulation profile. Additionally, higher viral load (<em>AOR</em> = 2.98, 95 % CI = 1.53–5.24) and injecting methamphetamine (<em>AOR</em> = 5.45, 95 % CI = 1.34–17.78) were associated with having a high gut-immune dysregulation profile.</div></div><div><h3>Conclusions</h3><div>Distinct patterns of microbial translocation, immune activation, inflammation, and metabolism of amino acid precursors distinguished gut-immune phenotypes of PWH reporting injection methamphetamine use and greater internalized stigma. Interventions tailored to PWH who inject methamphetamine or struggle with internalized stigma could optimize HIV-related health outcomes.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"51 ","pages":"Article 101156"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145712257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Levels of matrix metalloproteinase 9 (MMP-9) are elevated in persons with major depressive disorder who have had a recent suicide attempt","authors":"Faith Dickerson ,&nbsp;Emily Katsafanas ,&nbsp;Andrea Origoni ,&nbsp;Kelly Rowe ,&nbsp;Sabahat Khan ,&nbsp;Fahad Mukhtar ,&nbsp;Shuojja Yang ,&nbsp;Victor W. Splan ,&nbsp;Robert Yolken","doi":"10.1016/j.bbih.2025.101163","DOIUrl":"10.1016/j.bbih.2025.101163","url":null,"abstract":"<div><div>Matrix metalloproteinases (MMPs) are a diverse set of enzymes associated with tissue remodeling as well as inflammation and tissue destruction. MMP-9 is of interest since it has been associated with psychiatric disorders including major depressive disorder (MDD). Suicide attempts are a major complication of MDD. However, the association between MMP-9 levels and suicide attempts has not been extensively studied in persons with MDD. Sensitive enzyme immunoassays were employed to measure the levels of MMP-9 in blood samples from 186 persons with MDD receiving hospital care, 92 with a suicide attempt within the previous 30 days and 94 without a recent attempt, as well as 79 persons without a psychiatric disorder. Lifetime suicide attempt history in the MDD group was also recorded. Mixed effects models were employed to compare the MMP-9 levels among the groups adjusted for demographic and clinical variables. Wald tests were used to calculate pairwise comparisons. Employing these models, we found that individuals with MDD and a recent suicide attempt had higher levels of MMP-9 than individuals with MDD without a recent suicide attempt as well as individuals without a psychiatric disorder. There was not a significant difference in MMP-9 levels between the non-psychiatric group and individuals with MDD without a recent suicide attempt, regardless of whether they had a lifetime suicide attempt. Therapeutic modalities to modulate MMP-9 activity are currently being developed. The measurement of MMP-9 might be used to inform future clinical trials of these modalities for the prevention of suicide behaviors in high-risk individuals.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"51 ","pages":"Article 101163"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145939224","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic nanoliposome vaccine targeting multiple Aβ and tau epitopes reduces AD-like brain pathologies and rescues cognitive deficits in 3xTg-AD mice","authors":"Chun-Ling Dai ,&nbsp;Yiting Song ,&nbsp;Yonghua Chen ,&nbsp;Yunn Chyn Tung ,&nbsp;Wei-Chiao Huang ,&nbsp;Cheng-Xin Gong ,&nbsp;Jonathan F. Lovell","doi":"10.1016/j.bbih.2025.101167","DOIUrl":"10.1016/j.bbih.2025.101167","url":null,"abstract":"<div><div>Amyloid beta (Aβ) plaques and hyperphosphorylated tau neurofibrillary tangles (NFTs) are the histopathological hallmarks of Alzheimer's disease (AD) and targets for AD therapeutics. Since Aβ and tau pathologies both drive AD pathogenesis and progression, immunotherapies singularly targeting either Aβ or tau may be limited, and simultaneously targeting multiple epitopes of both Aβ and tau may be an efficacious approach. We developed a novel vaccine including three his-tagged tau peptides, tau_1-22, mid-region tau_171-191 (tau_pT181), and tau_388-407 (tau_pS396/S404), as well as two his-tagged Aβ fragments (N-terminal Aβ_1-14 and N-terminal pyroglutamate Aβ_pE3-14) with the spontaneous nanoliposome antigen particle (SNAP) system, termed SNAP-AD₅. Intramuscular vaccination of nine to ten months old of 3xTg-AD mice and age-matched wild-type control animals with SNAP-AD₅ or adjuvant only, once every three weeks for a total of 5 immunizations, simultaneously produced IgG titers of antibody against their specific antigens, significantly decreased Aβ and tau pathologies, and effectively improved cognitive function. SNAP-AD₅ was well tolerated without any detectable adverse side effects, including inflammatory responses in the peripheral circulation and in the brain, and hemorrhages in the mouse brain. These results support that SNAP-AD₅ simultaneously targeting both Aβ and tau is potentially a promising new approach for treating AD. Further optimization and development of the SNAP-AD₅ vaccine for treating AD is warranted.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"51 ","pages":"Article 101167"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145939125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Self-reported health and health literacy, neuroplasticity and neuro-immunological markers during the first 12 months in newly diagnosed people living with HIV: An exploratory study","authors":"Bengt B. Arnetz ,&nbsp;Judith E. Arnetz ,&nbsp;Norbert Kaminski ,&nbsp;Ryan Tomlin ,&nbsp;Pamela Bartlett ,&nbsp;Robert Crawford ,&nbsp;Andrew Jameson","doi":"10.1016/j.bbih.2025.101162","DOIUrl":"10.1016/j.bbih.2025.101162","url":null,"abstract":"<div><h3>Background</h3><div>There is limited description of dynamic changes in stress, inflammation, neuroplasticity, and health literacy during the early phase of HIV infection. This study examined patterns in self-reported stress, neurobiological and neuroplastic markers during the initial 12 months of living with HIV. The study also evaluated possible changes in functional health literacy, that is, patients’ ability to adhere to combination antiretroviral treatment (cART).</div></div><div><h3>Methods</h3><div>This is an observational cohort study of one female and eleven male and patients with newly diagnosed HIV attending an urban Ryan White funded HIV clinic. Participants responded to a survey and blood was drawn at baseline, and after 1, 3, 6, 9 and 12 months, respectively. The survey measured stress, depression, and health literacy. Blood was analyzed for HIV RNA plasma viral load, CD4 cell count, and biomarkers of stress, inflammation, and neuroplasticity.</div></div><div><h3>Results</h3><div>Viral load decreased from an initial mean count of 353,714.83 (S.E. 251,243.96) copies/mL to 24.54 (2.01) at 12 months (Wilcoxon Signed Rank Test, p = .012). CD4 cell count increased from 321.08 (48.49) to 541.13 (50.27) cells/mm³ (p = .012). Self-rated stress decreased from 6.83 (.92) to 4.81 (.96), on a 0–10 visual analogue scale (p = .043). Cumulative levels of C-reactive protein (CRP) were inversely associated with cumulative health literacy scores during the 12-month study (Spearman's rho = - 0.634, p = .025).</div></div><div><h3>Conclusion</h3><div>The study confirms that during the initial 12 months living with HIV, apart from the expected improvement in viral load and CD4, there is a significant decrease in self-perceived stress, but little changes in systems inflammation. The finding of an inverse relationship between levels of a pro-inflammatory marker and health literacy requires further studies.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"51 ","pages":"Article 101162"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145939124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A systematic review of the neurobiological mechanisms of chemotherapy-induced deficits in executive functions","authors":"Weiye Chen,&nbsp;Ian N. Johnston","doi":"10.1016/j.bbih.2025.101161","DOIUrl":"10.1016/j.bbih.2025.101161","url":null,"abstract":"<div><div>A subset of cancer patients and survivors experience cognitive decline during and after chemotherapy, a condition known as chemotherapy-induced cognitive impairment (CICI). Among the most affected domains are executive functions (EFs) - a set of higher-order cognitive processes essential for goal-directed behaviour, including working memory, behavioural flexibility, and inhibition. Emerging evidence suggests that these domains are differentially susceptible to chemotherapy drugs, implicating the selective disruption of distinct neural circuits and neurochemical pathways. To better understand the underlying mechanisms, we conducted a systematic review of rodent models of CICI, focusing on neurobiological alterations associated with chemotherapy and their relationship to EF deficits. A comprehensive search across PubMed, Web of Science, Scopus, and PsycINFO identified 67 eligible papers. Across studies, working memory and problem-solving impairments were most frequently examined and showed the greatest overlap across multiple mechanistic categories, including oxidative stress, mitochondrial dysfunction, neuroimmune dysregulation, impaired plasticity, and altered white matter integrity. Behavioural flexibility was most often linked to disrupted neurogenesis and metabolic imbalance, whereas attention and inhibition showed variable associations with neurotransmission and synaptic markers. Considerable heterogeneity within mechanistic categories reflected interactions among treatment regimen, animal sex, strain, and timing of assessment. Future studies should integrate molecular, cellular, and systems-level analyses within longitudinal and sex-balanced designs to clarify causal mechanisms and guide targeted interventions for preserving cognitive health in cancer survivors.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"51 ","pages":"Article 101161"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145939122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of combined prenatal exposure to air pollution and maternal stress on immune and dopaminergic gene expression in the gut-brain axis","authors":"Elise M. Martin,&nbsp;Matthew J. Morales,&nbsp;Niki Y. Li,&nbsp;Maura C. Stoehr,&nbsp;Matthew J. Kern,&nbsp;Madeline F. Winters,&nbsp;Caroline J. Smith","doi":"10.1016/j.bbih.2025.101165","DOIUrl":"10.1016/j.bbih.2025.101165","url":null,"abstract":"<div><div>Air pollution and maternal stress during pregnancy are both risk factors for neurodevelopmental disorders and often converge on the same communities. Epidemiological and animal studies suggest that maternal psychosocial stress may worsen the effects of air pollutants on neurodevelopmental outcomes. Previous work utilizing a mouse model of combined prenatal exposure to diesel exhaust particles (DEP) and maternal stress (MS) has found numerous sex-specific effects of DEP/MS exposure on neuroimmune outcomes, dopamine receptors, the gut-brain axis, and social behavior. However, it is unclear how broadly the immune landscape is shifted in the brain and intestinal epithelium following DEP/MS. Here, we analyzed immune gene expression in 5 brain regions important for social behavior and in 3 regions of the intestinal epithelium in both male and female offspring at ∼postnatal day 50, following either DEP/MS or control exposure. We found several interesting overall patterns. First, changes in expression of immune genes such as <em>CD11b</em> and <em>Tlr4</em> were concentrated in the nucleus accumbens and hippocampus. <em>Tlr4</em> and <em>Il-17ra</em> mRNA also increased in the jejunum and colon following DEP/MS, but only in females. Second, in the nucleus accumbens, catecholamine-O-methyltransferase (<em>Comt</em>) and dopamine transporter 1 (<em>Slc6a3</em>) gene expression were increased following DEP/MS, indicating increased dopamine degradation at and reuptake from the synapse, respectively. Additionally, dopamine D2 receptor (<em>Drd2</em>) mRNA was decreased following DEP/MS in males. Finally, we observed numerous sex differences in immune gene expression regardless of treatment in both the brain and gut. Together, these findings suggest the nucleus accumbens is a key site for neuroimmune and dopaminergic changes following DEP/MS exposure and indicate female-specific changes in intestinal immunity in young adulthood following these prenatal exposures.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"51 ","pages":"Article 101165"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145939222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Psychological distress predicts disease activity in inflammatory bowel disease: Results from the mind-body IBD longitudinal study","authors":"Natasha Seaton ,&nbsp;Joanna L. Hudson ,&nbsp;Valeria Mondelli ,&nbsp;Leah Raymond ,&nbsp;Pooja Schmill ,&nbsp;Ailsa Hart ,&nbsp;Rona Moss-Morris","doi":"10.1016/j.bbih.2025.101147","DOIUrl":"10.1016/j.bbih.2025.101147","url":null,"abstract":"<div><h3>Background &amp; aims</h3><div>Psychological distress (depression, anxiety, stress) is common in inflammatory bowel disease (IBD) and is linked to poorer outcomes, yet behavioural pathways and economic consequences remain unclear. This study tested a gut-brain-behaviour-outcome (GBBO) framework, testing: 1) reciprocal links between distress and disease activity; 2) whether health behaviours mediate distress-disease activity relationships; 3) if distress and self-reported disease activity (SRDA) predict adverse disease outcomes, controlling for inflammation and 4) whether disease activity mediates relationships between distress and adverse outcomes.</div></div><div><h3>Methods</h3><div>IBD patients (n = 157) reported distress, health behaviours, SRDA, healthcare use and disease-related outcomes at 3 waves at 6-month intervals. Faecal calprotectin (FCP) was assayed at baseline and 6 months. Analyses were conducted using structural equation modelling and mixed-effects models.</div></div><div><h3>Results</h3><div>Baseline distress predicted higher SRDA six months later (β = 0.16, <em>p=.</em>03) but did not predict FCP; reverse pathways were nonsignificant. Impaired sleep quality mediated 55 % of the effect of distress on future SRDA (β = 0.09, <em>p=.</em>04). Other behaviours were nonsignificant. Controlling for FCP, distress and SRDA independently predicted secondary healthcare usage (primary/secondary care) and disease-related outcomes (flare frequency/severity, absenteeism and productivity loss). FCP was positively related to flare frequency/severity and allied health practitioner visits only. Mediation analysis showed that SRDA partially mediated absenteeism.</div></div><div><h3>Conclusions</h3><div>Psychological distress exacerbates symptoms and economic cost. Poor sleep partially mediates the relationship between distress and SRDA, but not inflammation. Psychological interventions that focus on improving sleep could be cost-effective ways to improve mental health and symptom burden, with downstream impact on healthcare utilisation and productivity losses.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"51 ","pages":"Article 101147"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145746985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inflammatory profiles of transdiagnostic symptom dimensions in healthy females","authors":"Alicia J. Smith ,&nbsp;Stacey Kigar ,&nbsp;Quentin Dercon ,&nbsp;Mary-Ellen Lynall ,&nbsp;Konstantinos Ioannidis ,&nbsp;Muzaffer Kaser ,&nbsp;Caitlin Hitchcock ,&nbsp;Tim Dalgleish ,&nbsp;Camilla L. Nord","doi":"10.1016/j.bbih.2025.101146","DOIUrl":"10.1016/j.bbih.2025.101146","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Psychiatric disorders are increasingly conceptualised as heterogeneous categories with transdiagnostic underlying mechanisms that cut across multiple diagnoses and vary within a single diagnosis. Inflammation induced by psychosocial stress is one particularly potent example: previous research suggests that inflammatory profiles may correspond to symptom subgroups rather than traditional diagnostic categories. However, robust identification of transdiagnostic symptoms linked to specific inflammatory profiles remains rare. In this study, we examined the relationship between inflammatory profiles (at baseline and after a stress induction) and transdiagnostic symptom dimensions in females, who show higher prevalence of stress-related disorders such as anxiety and depression.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;A modest but relatively homogenous healthy female sample, between the ages of 18 and 35, was recruited (N = 26). We obtained venous blood samples, at baseline and after a combined physiological and social stress induction, to measure full blood counts, plasma cytokines and peripheral blood mononuclear cells (PBMCs; for cell stimulation and intracellular flow cytometry analysis). Participants completed a battery of psychiatric self-report questions, from which we modelled three transdiagnostic factor scores. Finally, we used Bayesian regressions to evaluate the predictive contribution of transdiagnostic factors to inflammatory markers (at baseline and stress-induced), as well as to the principal components of inflammatory measures (derived from a principal component analysis (PCA) of the inflammatory data).&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;We identified specific relationships between inflammatory profiles and transdiagnostic symptom dimensions. Higher scores on a ‘social withdrawal’ factor were associated with greater baseline neutrophil (95 % highest density interval (HDI) = [0.06, 1.32]; BF&lt;sub&gt;10&lt;/sub&gt; = 2.92) and monocyte counts (95 % HDI = [0.29, 1.46]; BF&lt;sub&gt;10&lt;/sub&gt; = 19.08), whereas higher ‘anxious-depression’ scores were associated with a lower baseline monocyte count (95 % HDI = [-0.96, −0.02]; BF&lt;sub&gt;10&lt;/sub&gt; = 1.81) and a greater inflammatory response to stress (e.g., change in neutrophil scores from pre-to post stress induction: (95 % HDI = [0.18, 2.14]); BF&lt;sub&gt;10&lt;/sub&gt; = 5.66). We also found evidence for an association between the ‘social withdrawal’ factor and an immune principal component most strongly weighted by monocytes, basophils, and IL-6 (95 % HDI = [-1.14, −0.01]; BF&lt;sub&gt;10&lt;/sub&gt; = 1.88).&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;We find preliminary evidence that different transdiagnostic psychiatric symptom dimensions map onto specific inflammatory profiles, both at baseline and after a stress induction. This represents a proof-of-principle for the use of data-driven and hypothesis-driven approaches to identify and link transdiagnostic factors with inflammatory changes, which may be of ","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"50 ","pages":"Article 101146"},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145684162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}